Abstract Background: The study aims to investigate the expression level of Thrombospondin 2 (TSP2) in Gastric Cancer (GC) and determine the relationship between TSP2 and clinical characteristics and prognosis. Methods: The online database Gene Expression Profile Interactive Analysis (GEPIA) was used to analyze the mRNA expression level of TSP2 in GC. The Kaplan-Meier plotter prognostic analysis tool was used to evaluate the influence of TSP2 expression on clinical prognosis in GC patients. The expression level of TSP2 was analyzed in paraffin-embedded GC samples and adjacent normal tissues by immunohistochemistry. The relationship between clinicopathological characteristics and prognosis of GC patients. Next, the relationship between clinicopathological characteristics and prognosis of GC patients was assessed. Transwell experiment was used to evaluate the effect of TSP2 on the invasion and migration of HGC27 and AGS cells. Results: Compared with normal tissues, the expression of TSP2 mRNA in GC was significantly up-regulated, and it was closely related to the clinical stage of GC. The high expression of TSP2 significantly affected the OS, FP and PPS of patients with GC. Among them, the expression level of TSP2 did not affect the prognosis of patients with GC in N0 subgroup, but significantly affected the prognosis of patients with GC in N (1+2+3)subgroup. The protein expression level of TSP2 in GC tissue was significantly higher than in normal tissues (P<0.01). The overall survival (OS) rate of patients with high TSP2 expression was lower than the low TSP2 expression group ( P =0.013). Knockdown of TSP2 can significantly inhibit the growth of GC cells. Proliferation, migration, invasion ability, and TSP2 expression level significantly correlate with mismatch repair genes such as PMS2, MSH6, MSH2, and MLH1 ( P <0.05). Conclusion : The expression of TSP2 in GC is significantly increased, closely related to the metastasis and mismatch repair process of GC patients and affected GC patients' prognosis. It is a potential marker and treatment target for the prognosis of GC patients.
Outbreaks of diseases and death of Mandarin fish have been observed in Guangxi, China, since 2023. A bacterial strain (No. 20230510) was isolated from the kidneys of diseased Siniperca chuatsi. Artificial infection tests confirmed that this strain was responsible for the disease observed in S. chuatsi. The bacterium was subjected to morphological observations, pathological analysis, whole-genome sequencing (WGS), and antibiotic susceptibility testing. Artificial infection tests indicated that the mortality rate in high-concentration groups reached 100%, with an LD50 of 3.89×104 CFU/ml, suggesting significant bacterial virulence. WGS revealed that the bacterium consisted of a single circular DNA chromosome, with a total size of 8,123,106 bp and a GC content of 68.14%, comprising 7,638 coding sequences (CDSs), 72 tRNA genes, and 12 rRNA genes. Phylogenetic tree analysis and comparison with the NR database showed that the genome sequence of this strain (accession no. CP130742) had the highest similarity, at 99.98%, with the UTF1 gene sequence of Nocardia seriolae (accession no. GCF_002356035.1), leading to their classification in the same clade. Therefore, this bacterium was identified as N. seriolae. Comparison with the virulence factor database revealed that 403 CDSs in the bacterium's genome may be virulence genes; these genes were primarily associated with nutrient metabolism, regulatory factors, immune modulation, effector delivery systems, and exotoxins. Comparative analysis of chromosomal gene sequences indicated the presence of multiple types of antibiotic resistance genes. Antibiotic susceptibility testing showed that the bacterium was susceptible to nine antibiotics, including enrofloxacin, doxycycline, florfenicol, and sulfamethoxazole. Histopathological observations revealed varying degrees of chronic granulomatous lesions in the liver, spleen, kidneys, gills, and intestines, with the most severe lesions occurring in the kidneys. These findings confirm that the N. seriolae strain 20230510 is pathogenic and the causative agent of the mortality observed in S. chuatsi, providing crucial data support for further research on comprehensive control strategies against N. seriolae in S. chuatsi.
The breast milk microbiome could be a source of infant intestinal microbiota. Several studies have found that some breast milk is extremely low in bacteria or is even sterile. There are limited studies on the effect of milk without bacteria on the infant gut microbiota. The purpose of this study was to investigate the gut microbiota of infants fed with bacterial milk or sterile milk. Meanwhile, we attempted to find the cause of undetectable bacteria in milk.A total of 17 healthy pregnant women and 17 infants were enrolled in this study. Fecal samples were collected from full-term pregnant women. Milk samples and infant fecal samples were collected on the 14th postnatal day. Breast milk and fecal samples were examined using 16S rRNA sequencing technology. Pregnant women and infants were grouped according to milk with or without bacteria. To compare the differences in gut microbiota and clinical characteristics between groups.Bacteria were detected in 11 breast milk samples, and the bacterial detection rate was 64.7%. Infants fed with bacterial milk showed higher Shannon index and Simpson index (P = 0.020, P = 0.048), and their relative abundance of Lachnospirales, Lachnospiraceae and Eggerthellaceae was markedly higher. In addition, there were more bacterial associations in the co-occurrence network of infants fed with bacterial milk. Pregnant women with sterile and bacterial breast milk showed no significant differences in their clinical characteristics, and microbial composition and diversity.Some breast milk from healthy postpartum women failed to be sequenced due to low microbial DNA quantities or is sterile. Research is needed to explore the reasons for this phenomenon. Infants fed with bacterial milk had higher Alpha diversity and more complex microbiota networks. These findings provide novel insight into milk microbiota and infant gut microbiota.
Abstract Background The concerted regulation of placenta microbiota and the immune responses secures the occurrence and development of pregnancy, while few studies reported this correlation. This study aimed to explore the relationship between the placenta microbiota and immune regulation during pregnancy. Methods 26 healthy pregnant women scheduled for elective cesarean section in the First Affiliated Hospital of Jinan University who met the inclusion criteria were recruited. Placenta and peripheral venous blood samples were collected. Microbiota in placental tissue was detected using high-throughput sequencing. Flow cytometry was used to detect immune cells in placental tissue and peripheral venous blood. ELISA and Luminex liquid chip technology were used to detect the content of cytokines in placental tissue and peripheral venous blood, respectively. Results The placental microbiota has stimulating effects on the local immunity of the placenta and mainly stimulates the placental balance ratio CD56 + CD16+/CD56 + CD16 and the placental macrophages, that is, it plays the role of immune protection and supporting nutrition. The stimulating effect of placental microbiota on maternal systemic immunity mainly induces peripheral Treg cells and B lymphocytes. Conclusion The placental microbiota may be an important factor mediating local immune regulation in the placenta, and placental microbiota participates in the regulatory function of the maternal immune system.
Necrotic enteritis (NE) causes huge economic losses to the poultry industry. Probiotics are used as potential alternatives to antibiotics to prevent NE. It is known that Clostridium butyricum can act as a probiotic that can prevent infection. However, whether or not it exerts a beneficial effect on NE in chickens remain elusive. Therefore, we investigated the impact of C. butyricum on the immune response and intestinal microbiota during the development of NE in chickens, including the stage of basal diets, high fishmeal supplementation diets and Clostridium perfringens challenge. Chickens were divided into two groups from day 1 to 20: diets either with or without C. butyricum supplementation were allowed for each group. At day 20, the chickens were divided into four groups: C. perfringens challenged and unchallenged chickens with and without C. butyricum supplementation. All groups were fed a basal diet for 13 days, and thereafter a basal diet with 50% fishmeal from day 14 to 24. Chickens were infected with C. perfringens from day 21 to 23. At day 13, 20 and 24, samples were collected for analysis of the relative expression of immune response and intestinal mucosa barrier related genes and intestinal microbes. The results show that C. butyricum can inhibited the increase of IL-17A gene expression and reduction of Claudin-1 gene induced-expression caused by C. perfringens challenge. Moreover, C. butyricum was found to increase the expression of anti-inflammatory IL-10 in infected chickens. Although C. butyricum was found to have a significant beneficial effect on the structure of intestinal bacteria in the basal diet groups and decrease the abundance of C. perfringens in the gut, it could not significantly affect the occurrence of intestinal lesions and was not significantly correct the shift in gut bacterial composition post C. perfringens infection. In conclusion, although C. butyricum promotes the expression of anti-inflammatory and tight junction protein genes and inhibits pro-inflammatory genes in C. perfringens challenged chickens, it is not adequate to improve the structure of intestinal microbiota in NE chickens. Therefore, more effective schemes of C. butyricum supplementation to prevent and treat NE in chickens need to be identified.
Background Probiotic supplementation has been popular and widespread, yet we still lack a comprehensive understanding of how probiotic supplementation during pregnancy affects the gut microbial networks of pregnant women and infants. In this study, we firstly used network analysis to compare the gut microbiota of pregnant women with and without probiotic supplementation, as well as their infants. Methods Thirty-one pairs of healthy pregnant women and infants were recruited and randomly divided into the probiotic group (15 mother-infant pairs) and the control group (16 mother-infant pairs). Pregnant women in the probiotic group consumed combined probiotics from 32 weeks to delivery. Fecal samples were collected from pregnant women and infants at several time points. Gut microbiota was evaluated using 16S rRNA gene sequencing. Intestinal microbial network and topological properties were performed using the molecular ecological network analysis. Results No significant difference was found between the probiotic and control groups on the microbial alpha and beta diversity. As the gestational age increased, the total links, average degree, average clustering coefficient, robustness, and the proportion of positive correlations were increased in pregnant women with probiotics administration. In contrast, these indices were decreased in infants in the probiotic group. Conclusion Probiotic supplement does not change the microbial diversity of pregnant women and infants, but significantly alters the intestinal microbial network structure and properties. Although pregnant women have more complicated and stable networks after probiotic administration, their infants have less stable networks.
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